MSC Neuro 2025 P1
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Feature |
Vermislesion(Static- |
Hemispherelesion |
|
Locomotor) |
(Dynamic) |
Speech& |
|
|
writing |
Oftennormal |
Dysarthria,megalographia |
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Finger–nose,heel–knee, |
Tests |
Romberg, Babinski asynergy |
RAM |
Eyesigns |
Nystagmus(anyform) |
Nystagmuspossible |
Muscletone |
↓Hypotonia |
↓Hypotonia |
Exampearls:
Cerebellarvssensoryataxia:CerebellarpersistswitheyesOPEN,sensoryworse witheyesCLOSED.
Speech,handwriting, nystagmus=cerebellarhemisphere.
Drunkengait,truncalinstability=vermis.
26.Sensitiveataxia. Clinicalcharacteristicsandfeatures.
27.Corticalandvestibularataxia. Clinicalcharacteristicsandfeatures.
TypesofAtaxia(ComparisonTable)
Type |
Localization/Lesion |
|
site |
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Posteriorcolumnsof |
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spinalcord,posterior |
|
roots,peripheral |
Sensitive |
nerves,brainstem |
(Posterior |
sensorypathways, |
Columna |
thalamus,parietal |
rAtaxia) |
cortex |
ClinicalFeatures
–Stamping/tabetic gait(liftsfeethigh, slapsfloorhard)
–Severeinstability indark/eyesclosed
–PositiveRomberg sign(visiongreatly improvesbalance)
–Lossofvibration&
KeyDistinguishingSigns
–Vision- dependent(improves witheyesopen, worsensclosed)
–Deepsensoryloss
–Typicallyno nystagmus,novertigo
Type |
Localization/Lesion |
ClinicalFeatures |
KeyDistinguishingSigns |
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site |
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positionsense |
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–Dysmetriain |
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coordinationtests |
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–Severevertigowith |
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senseofspinningof |
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environment |
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–Horizontal |
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nystagmus |
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–Nausea,vomiting, |
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sweating |
–Systemicvertigois |
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–Patientstaggers, |
hallmark |
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fallstowardssideof |
–Alwaysfallsinafixed |
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lesion(inRomberg |
direction |
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Vestibularapparatus |
alwaysdeviatesin |
–Eyesigns:horizontal |
|
(labyrinth),vestibular |
samedirection) |
nystagmus |
|
nerve(VIII),vestibular |
–Sometimes |
–Nosensoryloss,limb |
Vestibula |
nuclei,brainstem |
hearing |
coordinationusually |
rAtaxia |
vestibularpathways |
loss/tinnitus |
preserved |
|
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–Instability,esp. |
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whilewalking |
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andturning(fallsto |
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oppositesideof |
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lesion) |
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–Astasia-abasia |
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(can’tstand/walkin |
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severecases) |
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–Often |
–Deviationoppositethe |
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Frontallobe |
accompanied |
lesion |
|
(fronto-ponto-cerebella |
byfrontallobe |
–Associatedcortical |
|
rtract)or |
signs: grasping |
signs(frontalrelease |
|
temporo-occipital |
reflex,apraxia, |
reflexes,hemianopia, |
|
cortex → |
personality/behavio |
hallucinationsif |
Cortical |
cortico-cerebellar |
rchange,motor |
temporal/occipital)<br> |
Ataxia |
connections |
aphasia |
–Notimprovedbyvision |
Quickmnemonics
Sensitive ataxia=“Stamping gait,Sightsaves” (visiondependency)
Vestibularataxia=“Vertigo+Vomiting+(horizontal)Visionjerk(nystagmus)”
Cortical ataxia =“Cortexsigns+Contralateral deviation”
Soinexams:
Sensitive →sensorypathwaylesion,Rombergpositive,improveswithvision.
Vestibular→vertigo,horizontalnystagmus,falls tosameside.
Cortical→fallstooppositeside,withfrontal/temporallobesigns.
28.Methodologyforthestudyofcoordinationdisorders.
Methodology fortheStudyofCoordination(CerebellarFunctionExam)
The cerebellumcoordinatesposture,gait,voluntarymovements, muscletone, andspeech.Ipsilateralsignsiflesionincerebellarhemisphere.
1.Gait
Walkstraightline,eyes open→thenclosed.
Cerebellarataxia:wide-based,staggering,“drunken/sailorgait.”
Sensitive ataxia:stampinggait,worsenswitheyesclosed(Romberg+).
Vestibularataxia:fall toonesidewithvertigo,nystagmus.
Flankgait:side stepping→instability.
Turningquickly→staggeringincerebellarlesion.
2.Balance/Romberg’s Test
Patientfeettogether,armsforward,eyesclosed.
Cerebellarlesion: swayingwitheyesopen &closed(unlikesensoryataxia).
ComplicatedRomberg:tandemstance(heel-toe).
3.CoordinationTests(LimbAtaxia)
Finger–NoseTest:attarget,intentiontremor,overshoot.
Heel–KneeTest:heelslideso tibia→ataxia.
PointingTest/ReboundPhenomenon:arm overshootstarget,lackof“check” (Stuart-Holmes).
Diadochokinesis:rapidalternatingsupination–pronation=clumsy,irregular
→adiadochokinesis.
DysmetriaTests:
Pronatortest:over-rotationofpalm(hypermetry).
Schilder’stest:armdropsbelowtarget.
Hammertest:poorgrip alternation.
4.HandwritingTest
Askpatienttowritesentence /drawcircle.
Finding:irregular, large letters(megalographia).
5.Speech
Cerebellardysarthria:
Slowed,explosive,unevenstress
“Scanning/chantingspeech.”
6.Nystagmus
Horizontal/verticalfinejerksduringsideorupgaze.
Reflectsdisturbedcerebello-vestibularconnections.
7.MuscleTone
Hypotonia:limbssoft,pendularreflexes,increasedjointmobility.
8.Asynergy Tests(lossofsynergisticmovement)
Babinski’sAsynergy Test:
Supine,armscrossed;trytositup→legsliftinstead,trunkcannot.
Standingtest:patientfallsbackwardwhenheadisthrownback.
SummaryofKeyClinicalFeaturesof CerebellarLesion
Ataxia:imbalance, drunkengait
Dysmetria:overshoot/ undershoot
Dysdiadochokinesis: pooralternatingmovements
IntentionTremor:worsenswithtargetapproach
Nystagmus: horizontalorvertical
Dysarthria:scanning,irregularspeech
Hypotonia:pendularreflexes,floppymuscles
Asynergy:failure ofcoordinatedmultistepactions
Exampearl:
Di erentiateataxias: Sensory(visionhelps),Vestibular(vertigo,nystagmus,fallto oneside),Cerebellar(presentevenwitheyesopen+hypotonia, dysarthria, intentiontremor).
29.Thepallidarsystem anditsdamage. Parkinsonism.
Pallidar(Extrapyramidal)System
PartoftheExtrapyramidal(strio-pallidar)system,responsible forautomatic stereotypedmovements(habitual,subconscious,energy-sparing).
Ensuressmoothchangeofcontraction →relaxation,motorautomatisms,posture, tone.
Anatomy
Striatal(younger):Caudatenucleus+Putamen
Pallidal(older):Globuspallidus(internal&external),Subthalamicnucleus(ofLuys), Substantianigra,Rednucleus.
Closelyconnectedto:frontalcortex, thalamus,brainstemnuclei,cerebellum.
Maine erents:pallido-reticular-spinal,nigro-reticular-spinal,rubro-spinal, tectospinal,vestibulospinaletc.
SyndromologyofPallidarLesions
PallidarSyndrome=Hypertensive-hypokineticsyndrome=Parkinsonism
Etiology
Degenerationofsubstantianigra /pallidum→ dopaminedeficiency
Causes:idiopathic(Parkinson’sdisease),post-encephalitic,atherosclerosisof basalganglia,toxins(CO,Mn,Pb,Hg, neuroleptics),trauma,tumors,hereditary disorders.
ClinicalPictureofParkinsonism
1.Hypokinesia/Bradykinesia
Povertyofmovements(oligokinesia)
Di icultyinitiating→“freezing,”“markingtime”beforewalking
Slowexecution(bradykinesia)
Reducedfacialexpression(amimia)
Reducedgesticulation/ arm swing(acheirokinesis)
2.PostureandGait
Stooped“beggar’s”posture:trunkbentforward,armsflexedatelbows
Smallshu lingsteps(festinatinggait)
Propulsion(fallsforward),Retropulsion(fallsbackward),Lateropulsion(falls toside)
“Paradoxicalkinesias”→suddennormalmovementsunderemotionalstress (patientcanrun/jumpunexpectedly)
3.MuscleTone
Plastichypertonia =“lead-piperigidity”
Withsuperimposedtremor→cogwheelrigidity
4.Tremor
Restingtremor,4–6Hz,“pill-rolling”offingers
Decreaseswithmovement,disappearsinsleep
5.Speech
Monotonous,quiet,slow(bradilalia)
6.Handwriting
Small,cramped,illegible(micrographia)
7.Autonomicchanges
Seborrhea/oilyface
Hypersalivation
Sweatingabnormalities
Skinpeeling
8.Othersigns
Sleep→tremor&rigiditydisappear
Slownessofthought(bradyphrenia)mayaccompany
SummaryTable:ParkinsonismClinicalFeatures
Group |
Features |
Motor |
Bradykinesia,di iculty startingmovement,festinatinggait, |
(hypokinetic) |
decreasedarmswing,amimia |
Postural |
Stoopedposture,propulsion/retropulsion/lateropulsion |
Tone |
Rigidity:lead-pipe/cogwheel |
Kinetic |
|
Disorders |
Tremor atrest(“pill-rolling”),disappearsinsleep |
Voice &Writing |
Monotonous,quietspeech(bradilalia);Micrographia |
Autonomic |
Seborrhea,hypersalivation,sweatingdisorders |
Special |
|
phenomena |
Paradoxicalkinesias(suddennormalmovements) |
Management
Pharmacological:
Dopamineprecursors(Levodopa+Carbidopa/Benserazide)
Dopamineagonists(bromocriptine,ropinirole,pramipexole)
MAO-Binhibitors(selegiline,rasagiline)
COMTinhibitors(entacapone)
Anticholinergics(trihexyphenidyl)— reducetremor
Supportive:physiotherapy,speechtherapy
Surgery(nowrare,replacedbyDBS):
Deepbrainstimulation(DBS,STN/GPitarget)
Historicpallidotomy/thalamotomy
ClinicalPearl:
Pallidarlesions→hypokinetic-hypertonicsyndrome=Parkinsonism
Striatallesions(Caudate+Putamen)→usuallyhyperkineticsyndromes(chorea, athetosis).
30.Striarsystem,themaintypesofhyperkinesis.
Striatal(Neostriatal)System
Evolutionary:Phylogenetically“newer”(neostriatum).
Structures:
1.Caudatenucleus
2.Putamen(shell)
3.Amygdala
4.Claustrum (fence) Connections
Striatumreceivesa erentsfromcortex, thalamus,substantianigra.
Regulatesmuscletone,posture,initiationofautomaticmovements.
Neurotransmitters:dopamine,serotonin,acetylcholine,GABAetc.
SyndromologyofStriatalLesions
Unlikepallidallesions(which→ Parkinsonism=hypokinetic-hypertonic),striatallesions mainlyproducehyperkineticsyndromes.
1.HyperkineticSyndromes
Definition:Involuntary,excessive,purposelessmovements,occuragainstthewill,not suppressible.
Types
Chorea–irregular,flowing,jerkymovementsfromone musclegrouptoanother(“St. Vitusdance”),lookslikerestlessness.
Athetosis–slow,writhing,worm-likefingermovements;mayextendtotrunk.
Ifgeneralized→torsionspasm(spasmodictwistingofbody).
Choreoathetosis–mixedtype.
Ballism–violentflingingmovementsofproximallimbs(hemiballismusifoneside, lesionusuallyin subthalamicnucleus).
Tics–suddenstereotypedmovements(facialtwitch,eyeblinking,grimacing, hemispasm,paraspasm).
Myoclonus–lightning-likemusclejerks(localorgeneralized).
Habitspasm–stereotypicrepetitive movements.
Torticollis(spasmodic wryneck)–duetoSCMspasm;improvedbytactile stimulus (Wartenberg’sgesture).
Generalfeaturesofhyperkinesia:
Reducedmuscletone(unlikepallidalrigidity).
Disappearduringsleep.
Individualrhythmicity, variable amplitude andpattern.
2.Hypokinetic/DystonicSyndromes
Lesscommonin striatallesions,butmayoccur:
Dystonia:abnormal prolongedmusclecontraction→abnormal posture (torsiondystonia).
Rigidity+hypokinesia canoverlapifpallidalpathwaysinvolved.
ClinicalFeaturesof StriatalDamage
Hyperkinesia=chieffeature:chorea,athetosis,ballism,tics.
Coordinationtestsmay showdysmetria,adiadochokinesis(butmuch lessthantrue cerebellarataxia).
Gait:varies(choreic,writhing,“waddling,”“cockgait,”pretentious/elaborategait).
Speech:scanning, explosive(duetoincoordination).
Tone: usuallyhypotonia,exceptindystonicforms(torsionspasmwithrigidity).
SummaryTable:StriatalvsPallidalSyndromes |
|
|
Feature |
Striatal |
Pallidallesion(globus |
|
lesion(caudate/putamen) |
pallidus,substantianigra) |
Dominant |
|
Hypokinetic- |
syndrome |
Hyperkinetic |
hypertonic(Parkinsonism) |
|
Chorea,athetosis,ballism, |
|
|
tics,torsiondystonia, |
Bradykinesia, rigidity,resting |
Movements |
myoclonus |
tremor, micrographia |
|
↓Hypotonia(exceptdystonia↑ |
|
Tone |
tone) |
↑Plastic“lead-pipe”rigidity |
|
“Dance-like,”writhing, bizarre |
Stooped,shu linggait, |
Posture/gait |
gait |
propulsion/retropulsion |
Speech |
Scanning,jerky |
Monotone,soft(bradilalia) |
Writing |
Large,uneven |
Micrographia |
|
Huntington’sdisease,Wilson’s |
Parkinson’sdisease,post- |
Typical |
disease,Sydenham’schorea, |
encephalitic, toxins, |
cause |
stroke(subthalamus→ballism) |
vascularlesions |
ExamPearl: